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Abstract

Objective: Chemerin and resistin are pro-inflammatory cytokines that have been shown to play a role in atherosclerosis and coronary artery disease. However, their association with carotid atherosclerosis has not been investigated. We sought to assess the relationship between a) circulating chemerin/resistin levels and cerebrovascular symptomatology, and b) chemerin/resistin plaque expression and carotid plaque instability.

Methods: Patients scheduled for carotid endarterectomy were recruited from the Royal Victoria and Jewish General hospitals, Montreal, Canada. Blood was drawn pre-operatively and plasma resistin and chemerin were measured using ELISA. Maximum stenosis sections were stained with hematoxylin and eosin and immunostained with anti-CD3 and anti-CD68. Two vascular pathologists used semi-quantitative scales to classify plaque foam cells and inflammatory cells as well as overall plaque instability. RNA was isolated from the area of maximum stenosis, reverse transcribed, and qPCR was performed to measure chemerin and resistin expression. Kruskal-Wallis or Mann-Whitney U tests were used to evaluate differences in resistin and chemerin between groups.

Results: In this ongoing study we recruited 169 patients (66.1% men, 74.5% symptomatic) with a mean±SD age of 70.0±9.3 years. To date all 169 patients had blood samples drawn and 100 had plaque chemerin and resistin expression assessed. Symptomatic patients had higher plasma chemerin (230 (179.0-261.3) vs. 201.4 (175.8-228.1) ng/ml, P=0.08) and resistin levels (12.7 (10.2-17.7) vs. 10.8 (7.1-16.0) ng/ml, P=0.02) when compared with asymptomatic patients. Chemerin plaque expression was decreased in plaques with greater number of foam cells and inflammatory cells and in plaques with greater overall instability. Resistin plaque expression was also decreased in plaques with a greater number of foam cells and inflammatory cells.

Conclusions: Circulating chemerin and resistin levels are increased in symptomatic patients. Intraplaque chemerin and resistin expression is inversely related to the number of plaque inflammatory cells and instability. Our ongoing work will determine the underlying mechanisms linking chemerin and resistin with atherosclerotic plaque instability.